Circadian rhythms govern diurnal variations in physiological functions and are synchronized by 24-h cyclic signals with light being often the main external cue (“Zeitgeber”). At the molecular level, in many species circadian clocks involve periodic changes in the expression of a canonical set of clock genes but involve also post-translational histone modifications. Schistosomes are important human parasites that cause Bilharziasis. Their reservoir hosts are rodents. Infective larvae (cercariae) are produced in vector snails and released into fresh water at specific time points corresponding to the principal activity of the vertebrate hosts: 12 AM for human hosts, 8 PM for rodents hosts. We show that the timing of cercarial shedding is not correlated with canonical clock gene expression but can be linked to modifications of H3K9/H3K14 acetylation. A Hidden Markov Model (HMM)-based approach identified 107 differentially acetylated regions containing 61 candidate genes of which at least 14 (23%) can be related to the control and establishment of circadian rhythm. This suggests a flexible histone acetylation based phasing mechanism for circadian shedding of Schistosoma mansoni cercariae that allows for rapid adaptation to host behavior. The zeitgeber for this system and its genetic determinants remain to be discovered.